Soluble TWEAK levels are independently associated with coronary artery disease severity in patients with stage 2–3 kidney disease

Azak, Alper; Akdoğan, Mehmet Fatih; Denizli, Nazım; Huddam, Bülent; Koçak, Gülay; Gücün, Murat; Tatlısu, Mustafa Adem; Demi̇rci̇, Recep; Yılmaz, Bilal; Dikeç, Mehmet; Bakırtaş, Murat; Akdağ, İ̇brahim; Duranay, Murat

doi:10.1007/s11255-013-0562-4

Cited by 8 publications

(10 citation statements)

References 17 publications

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“…In the literature, there are contradictory findings of the relationship between TWEAK levels and atherosclerosis (27,28). Previous studies showed a negative relationship between serum TWEAK levels and coronary artery disease, cIMT, insulin resistance, gestational diabetes and type II diabetes (29)(30)(31)(32). However, studies cannot explain the reason why atherosclerotic process accelerated when serum TWEAK levels were low (33).…”

Section: Discussionmentioning

confidence: 99%

Soluble Tumor Necrosis Factor (TNF)-Like Weak Inducer of Apoptosis (Tweak) Independently Predicts Subclinical Atherosclerosis in Behcet’s Disease

İçli̇

Cüre

Cüre³

et al. 2018

Acta Med. (Hradec Kralove, Czech Repub.)

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Background: Vasculopathy is a major cause of mortality and morbidity in Behcet’s Disease (BD). Subclinical atherosclerosis can even be detected in the early stage of BD. Soluble tumor necrosis factor-like (TNF) weak inducer of apoptosis (TWEAK) is known as a good marker of the inflammation in vascular tree. The aim of this study is to examine the relationship between carotid artery intima-media thickness (cIMT) and serum TWEAK levels in patients with BD. Materials and Methods: In line with International BD Study Group criteria, 48 BD, and 30 controls were included in our study. Disease activity was evaluated according to BD current activity form (BDCAF). C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), lipid parameters, serum TWEAK levels, and cIMT were measured. Results: Disease activity score of BD patients was found as 2 (range 0–7). cIMT, serum TWEAK, CRP and ESR levels of BD patients were significantly higher comparing to cIMT (0.62 ± 0.13 mm vs. 0.43 ± 0.09 mm, p < 0.001), serum TWEAK (667.5 ± 130.6 vs. 603.4 ± 89.6 pg/ml, p = 0.015), CRP (3.9 ± 4.3 vs. 1.4 ± 1.0 mg/dl, p < 0.001) and ESR (10.2 ± 10.0 vs. 5.6 ± 3.7 mm/h, p = 0.005) levels of the control group. There was a positive correlation between serum TWEAK level and disease activity (r = 0.251, p = 0.030) and cIMT (r = 0.463, p < 0.001). Our study also revealed an independent correlation between cIMT and serum TWEAK levels (beta = 0.354, p < 0.001). Conclusion: Increased serum TWEAK levels can play a part in the development of atherosclerotic heart disease in BD. Due to their liability to atherosclerosis, patients with BD must followed closely.

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Section: Discussionmentioning

confidence: 99%

Soluble Tumor Necrosis Factor (TNF)-Like Weak Inducer of Apoptosis (Tweak) Independently Predicts Subclinical Atherosclerosis in Behcet’s Disease

İçli̇

Cüre

Cüre³

et al. 2018

Acta Med. (Hradec Kralove, Czech Repub.)

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“…TNF-like weak inducer of apoptosis (TWEAK) was recently found to stimulate the expression of inflammatory cytokines locally in kidney cells and to down-regulate the expression of Klotho in vitro and in vivo [11]. Soluble TWEAK levels were independently associated with coronary artery disease severity in patients with stage 2-3 CKD [12]. …”

Section: Outcomes Of Inflammation In Ckdmentioning

confidence: 99%

Update on Inflammation in Chronic Kidney Disease

2015

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Background: Despite recent advances in chronic kidney disease (CKD) and end-stage renal disease (ESRD) management, morbidity and mortality in this population remain exceptionally high. Persistent, low-grade inflammation has been recognized as an important component of CKD, playing a unique role in its pathophysiology and being accountable in part for cardiovascular and all-cause mortality, as well as contributing to the development of protein-energy wasting. Summary: The variety of factors contribute to chronic inflammatory status in CKD, including increased production and decreased clearance of pro-inflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, including those related to dialysis access, altered metabolism of adipose tissue, and intestinal dysbiosis. Inflammation directly correlates with the glomerular filtration rate (GFR) in CKD and culminates in dialysis patients, where extracorporeal factors, such as impurities in dialysis water, microbiological quality of the dialysate, and bioincompatible factors in the dialysis circuit play an additional role. Genetic and epigenetic influences contributing to inflammatory activation in CKD are currently being intensively investigated. A number of interventions have been proposed to target inflammation in CKD, including lifestyle modifications, pharmacological agents, and optimization of dialysis. Importantly, some of these therapies have been recently tested in randomized controlled trials. Key Messages: Chronic inflammation should be regarded as a common comorbid condition in CKD and especially in dialysis patients. A number of interventions have been proven to be safe and effective in well-designed clinical studies. This includes such inexpensive approaches as modification of physical activity and dietary supplementation. Further investigations are needed to evaluate the effects of these interventions on hard outcomes, as well as to better understand the role of inflammation in selected CKD populations (e.g., in children).

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“…In addition to decreasing Klotho through epigenetic mechanisms, TWEAK directly promotes cardiac dysfunction and failure through downregulation of the mitochondrial biogenesis regulator PGC1α, an action of TWEAK that also contributes to CKD [52, 53], and increases vascular calcification [54]. In keeping with this, higher serum TWEAK levels are associated with the severity of coronary artery disease, particularly in CKD Stages 2 and 3 patients [55], and predict mortality in haemodialysis patients [56]. Liver TWEAK signalling is differentially activated by palm oil in association with insulin resistance [57] and in response to a high-fat diet, and it contributes to liver steatosis, fibrosis and inflammation and insulin resistance [58].…”

Section: Introductionmentioning

confidence: 99%

A journey from microenvironment to macroenvironment: the role of metaflammation and epigenetic changes in cardiorenal disease

Kanbay

Yerlikaya

Sag

et al. 2019

Clinical Kidney Journal

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Chronic non-communicable diseases have become a pandemic public problem in the 21st century, causing enormous burden on the economy, health and quality of life of societies. The role of a chronic inflammatory state in the pathogenesis of chronic disease has been more comprehensively recognized by recent findings. The new paradigm ‘metaflammation’ focuses on metabolism-induced (high fat or fructose-based diet or excessive calorie intake) chronic inflammation. There is a close correlation between the increased incidence of chronic kidney disease (CKD) and chronic heart failure with both increased inflammatory marker levels and western-type diet. In this review we describe the concept of metaflammation, its role in the development of CKD and chronic heart disease, the molecular and signalling pathways involved and the therapeutic consequences.

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Soluble TWEAK levels are independently associated with coronary artery disease severity in patients with stage 2–3 kidney disease

Abstract: Our results indicate a relationship between sTWEAK levels and CAD in CKD stages 2-3 patients.

Cited by 8 publications

References 17 publications

Soluble Tumor Necrosis Factor (TNF)-Like Weak Inducer of Apoptosis (Tweak) Independently Predicts Subclinical Atherosclerosis in Behcet’s Disease

Soluble Tumor Necrosis Factor (TNF)-Like Weak Inducer of Apoptosis (Tweak) Independently Predicts Subclinical Atherosclerosis in Behcet’s Disease

Update on Inflammation in Chronic Kidney Disease

A journey from microenvironment to macroenvironment: the role of metaflammation and epigenetic changes in cardiorenal disease

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